Abstract:
:Duchenne muscular dystrophy (DMD) is secondary to loss-of-function mutations in the dystrophin gene. The causes underlying the progression of DMD, differential muscle involvement, and the discrepancies in phenotypes among species with the same genetic defect are not understood. The mdx mouse, an animal model with dystrophin mutation, has a milder phenotype. This article reviews the available information on expression of signaling-related molecules in DMD and mdx. Extracellular matrix proteoglycans, growth factors, integrins, caveolin-3, and neuronal nitric oxide synthase expression do not show significant differences. Calcineurin is inconsistently activated in mdx. which is associated with lack of cardiomyopathy, compared to the permanent calcineurin activation in mdx/utrophin null mice that have a DMD-like cardiomyopathy. Levels of focal adhesion kinase (FAK) and extracellular regulated kinases (ERKs) differ among mdx and DMD. Further work is needed to identify the point of discrepancy in these signaling molecules' pathways in dystrophynopathies.
journal_name
Biol Resjournal_title
Biological researchauthors
Fadic Rdoi
10.4067/s0716-97602005000400010keywords:
subject
Has Abstractpub_date
2005-01-01 00:00:00pages
375-80issue
4eissn
0716-9760issn
0717-6287pii
S0716-97602005000400010journal_volume
38pub_type
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journal_title:Biological research
pub_type: 杂志文章
doi:10.4067/s0716-97602006000300010
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doi:/S0716-97602007000500009
更新日期:2007-01-01 00:00:00
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更新日期:2014-04-01 00:00:00
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doi:
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doi:
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journal_title:Biological research
pub_type: 杂志文章
doi:
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doi:/S0716-97602009000100013
更新日期:2009-01-01 00:00:00
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journal_title:Biological research
pub_type: 杂志文章,评审
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更新日期:1995-01-01 00:00:00
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doi:
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doi:/S0716-97602010000200013
更新日期:2010-01-01 00:00:00
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journal_title:Biological research
pub_type: 杂志文章,评审
doi:
更新日期:1998-01-01 00:00:00